Abstract
Obesity is well known to be a major cause of several chronic metabolic diseases, which can be partially counteracted by exercise. This is due, in part, to an upregulation of mitochondrial activity through increased nicotinamide adenine dinucleotide (NAD+). Recent studies have shown that NAD+ levels can be increased by using the NAD+ precursor, nicotinamide mononucleotide (NMN) leading to the suggestion that NMN could be a useful intervention in diet related metabolic disorders. In this study we compared the metabolic, and especially mitochondrial-associated, effects of exercise and NMN in ameliorating the consequences of high-fat diet (HFD) induced obesity in mice. Sixty female 5 week old C57BL6/J mice were allocated across five groups: Chow sedentary: CS; Chow exercise: CEX; HFD sedentary: HS; HFD NMN: HNMN; HFD exercise: HEX (12/group). After 6 weeks of diet, exercise groups underwent treadmill exercise (15 m/min for 45 min), 6 days per week for 6 weeks. NMN or vehicle (500 mg/kg body weight) was injected (i.p.) daily for the last 17 days. No significant alteration in body weight was observed in response to exercise or NMN. The HFD significantly altered adiposity, glucose tolerance, plasma insulin, NADH levels and citrate synthase activity in muscle and liver. HEX and HNMN groups both showed significantly improved glucose tolerance compared to the HS group. NAD+ levels were increased significantly both in muscle and liver by NMN whereas exercise increased NAD+ only in muscle. Both NMN and exercise ameliorated the HFD-induced reduction in liver citrate synthase activity. However, exercise, but not NMN, ameliorated citrate synthase activity in muscle. Overall these data suggest that while exercise and NMN-supplementation can induce similar reversal of the glucose intolerance induced by obesity, they are associated with tissue-specific effects and differential alterations to mitochondrial function in muscle and liver.
Highlights
Obesity is a global health issue with increasing prevalence
Dissected fat pads, muscles and liver were significantly higher in high-fat diet (HFD) sedentary animals compared to those consuming chow
In those consuming HFD, both nicotinamide mononucleotide (NMN) and exercise interventions reduced net liver mass (Table 1) but this difference did not remain after correction for body weight
Summary
Obesity is a global health issue with increasing prevalence. According to the WHO (2015), 1.9 billion adults were overweight globally in 2014, of which 0.6 billion were obese. In 2014, The McKinsey Global Institute reported that if the current growth rate continues, by 2030, almost half of the world’s adult population will be overweight or obese. The increasing prevalence of obesity leads to an increased risk of several other non-communicable diseases including type 2 diabetes, cardiovascular disease, some cancers, respiratory conditions, fatty liver disease, reproductive disorders, depression, and other mental health conditions (Gonçalves et al, 2012; Morris et al, 2014). The obesity epidemic can be explained as a result of energy imbalance. A variety of human and animal studies have suggested that exercise can exert health benefits in obesity (Christ et al, 2002; Flores et al, 2006; Vieira et al, 2009; Ross et al, 2015)
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